Good evening, everybody, and welcome to tonight's webinar. My name is Bruce Stevenson, and I have the honour and privilege of chairing tonight's session. I'd like to start off by giving a big thank you to our sponsors, Bailey's Horse Feeds for sponsoring tonight's session.

We really do appreciate the sponsorship. So thank you to Bailey's Horse Feeds. A little bit of housekeeping quickly for those of you that haven't been with us before.

If you move your mouse over the screen, you'll see a little control bar pops up. There's a Q&A box there. Click on that and just type away, and we will, get those and keep all those questions over to the end.

And Jonathan has very kindly agreed to answer as many of those as what time allows. Speaking of Jonathan, Jonathan Anderson is our presenter tonight and he's the director and equine surgery clinician at the Rainbow Equine Hospital. He is a Royal Veterinary College equine sur surgical specialist, a diplomat of the American College of Veterinary Surgeons, and an FEI accredited veterinary delegate for evening.

Jonathan graduated from the Royal Dick School of Veterinary Studies in 2000, completed an internship in Saint Louis Rey equine Hospital in California before making, making his way back to Rainbow Equine Hospital for 3 years. He completed an equine clinical fellowship at Oregon State Veterinary Teaching Hospital, followed by an equine surgical residency at the University of California, Davis. He achieved diplomat status in 2008, remained as a clinical instructor at UC Davis before moving back to the Rainbow Equine Hospital in 2009.

Jonathan performs arthroscopic and laparoscopic surgery regularly as part of his surgical responsibilities. Jonathan also lectures and publishes on his main interests of orthopaedic surgery, poor performance and lameness diagnosis, and has a specific interest in diagnosis and surgical treatment of cervical stenotic myelopathies. Jonathan, welcome back to the webinar vet and it's over to you.

Many thanks. So the aim of tonight's talk really is to discuss, cervical synotic myelopathy, otherwise known by most people as wobbler syndrome and horses, and to discuss really what we have, in terms of diagnostics that are new, update everyone on. That, but also really to look at the different treatment options, and not necessarily from the perspective of just a, a subjectively, but more of an evidence-based approach to this, in an effort to really see, can we be confident of what we're advising, owners and clients who have horses with this condition.

So as we move on, the, principal, reason that we see horses presenting with cervical synoptic, myelopathy or CBSM is ataxia. And, and ataxia comes in, in different forms. The infectious diseases, the multifocal diseases, both of which really we're not going to cover tonight.

They are of little consequence of. We don't really, see them, associated with disease in this country. We occasionally see motor neuron disease and equine degenerative myelopathy or EDM, but really my main focus of tonight's talk is is the compressive spinal cord diseases, which are usually resulting in, ataxia, as a result of the compression.

So, in terms of definition, cervical vertebral synotic myelopathy has been known, by different names, equine sensory ataxia, equine in coordination, or spinal ataxia, all of them really, demonstrating the, the fact that we are dealing with, some degree of spinal cord. Or inflammation leading to a physical manifestation of that. And this can be down to three, main, anatomical, reasons associated with the cervical spine, either a, a marticulation, a malformation, or indeed a malalignment of the cervical vertebral foramen.

As a result of that, resulting in some degree of either instability, or cervical compression, and as a result of that spinal cord, compression. This gives us the, the term wobbler because these horses are a toxic, they often look weak or wobbly, and it, it's not a new condition, as you can see from a Doctor Mayhew. You commented 1860, in his book, The Illustrated Horse, that with few exceptions, a wobbler is a permanent neurological gait deficit that renders a horse unsuitable for use.

Now, we would say, agree with their permanent neurological gait deficit, however, the unsuitable for use, definitely these days, we should not be bound by that 1860, definition. And so in doing so, I'd like to go through the presentation on clinical symptoms, then have a look at the diagnosis and in particular what we can do more to diagnose these and be comprehensive in it. And then finally at the treatment options that we have and looking at those, as I say, in an evidence-based way.

The two broad presentations of equine ataxia, when it's related to stenotic myelopathy, are in either mature horses or immature horses. And when I say mature horses, I mean horses that are greater than, between 2 and 4 years. So oftentimes horses over 4 years, i.e., horses that, whose growth plates that are generally speaking closed, versus immature horses who are usually in the sort of 18 months and less category.

With the more mature horses, often these horses are presenting with a stiff neck or a low neck carriage. They may have mild, to severe ataxia, but ataxia often can be one of the less common reasons for presentation. Sometimes these horses are lame, either 4 or hind them, and they may well have a history of an abnormal gait, an unusual gait, or a shifting what what is thought to be a shifting gait or a shifting lameness associated with a hind or.

For leg. Oftentimes, there'll be a loss of muscle, especially over the neck, hind limbs area. The immature horses, these horses are usually, young, unbroken, sometimes they'll just be broken.

They can often be profoundly attaxic, and often it's seen as a sudden onset of acute incidents. Very frequently, these horses will be, have lack of, a, a degree of muscleture on their neck that make them look like they have what I would term a pencil neck. Now also we can, we can broadly categorise the CVSM in two ways, looking at an unstable cervical column and in this case, the, the, the degree of stenosis as outlined by the, vertebra, by the blue lines here, the degree of stenosis is affected by the position of the neck.

So in the mid neck region, typically as flexion increases, we see a, a, a malarticulation or instability of the alignment of the ventral aspect of the spinal foramen that results in a step being created, and as you can see in the myelographic image at the bottom of the screen, where we have compression of the dye associated with the contrast column, in myelography. And because That malalignment, we have a compression of the spinal cord. This is often presented in between the C3, 4, and 5 regions of the neck, and are often seen in the younger horses.

And this is an unstable, malformation of the cervical spine. When the neck is in a neutral position, oftentimes that, spinal cord compression is not evident. This is, as opposed to the more static, myelopathy, when it's associated really irrespective of neck position, we end up with some degree of spinal cord compression, and that can be due to a range of, features, but normally, typically older horses with degenerative joint disease of the articular process joints, and typically we see this effect in the C5, C6.

T7 and the T1 articular processes. Because it's a degenerative process, we normally see it in older horses, but older horse in this instance is just reference to a mature horse, and, and certainly a horse greater than 4 years will be typically, is, is the, the age of horse that we're associated with. Even horses with 4 years, which is relatively young.

Horse can develop rather enlarged articular process joints resulting in this more static deformation of the spinal canal, and as a result, spinal cord compression that does not vary with position of the neck. And this certainly within the UK context is is the more frequent presentation that we see where degenerative joint disease is, is a more common sequela that we're seeing in these horses. It's helpful just to have a look at the types of remodelling that we can see associated with a cervical articular process.

On the left and the right of the picture, you'll see the the cervical articular processes, and you'll see on the, on the left of the stream where the ventral aspect of the articular process is enlarged, has remodelling of bone, and as a result, The gap between the vertebral foramen and the articular process is reduced. These are typical of osteophytes, that we get with any arthritic joint. We can also get synovi proliferation within the joint and cervical vertebral stenotic myelopathy can be the result in, in these instances.

Now the prevalence has been looked at and it and it's a relatively, it's a relatively low prevalence, of, of stenotic myelopathy. Now, in thoroughbred horses, it's a lot easier to look at this, where there's a far greater recording system being done. Whether that's in the States or in Europe, but this study in 2010 looked at 350,000 clinical records over seven years, and there was 3 farms in Europe and one in the USA with a total of just, over 1100, falls that were looked at.

And the prevalence really, was, was relatively low at 1.3%. However, that still means that 13 of 1000 horses will have, spinal cord ataxia.

Interestingly, type one, generally speaking, that's the dynamic compression. Between the age 6 weeks and, and sort of up to 2 years, over half of the horses were affected at that age, and this is typical in the thoroughbred, the thoroughbred environment, whereas the static form really between 3 and 3.5 years was seen in, in a quarter of cases.

Again, this is relatively, skewed because The thoroughbred horse population, obviously these horses are a lot younger when they start training, start working, and so as opposed to warm-blood horses, which we'll look at in a little bit more detail. And here you see that, in a couple of European studies, and one study that we did through Rainbow Queen Hospital, the distribution is a lot different, where warmblood horses accounted for 88% in that one study from Germany, and in our population of horses, 78% of them were warmbloods with a satching of other breeds and really a very low, prevalence of Thoroughbred horses, from an age perspective, really only 6% in, the, in the Slazar's study, and the less than, and 5% in our study were less than a year old, with far greater, over half in our population of horses, well over 60% of them being, over, over 5 years of age. And so in that respect, then, you know, our age and our breed distribution are far greater across, the, the warm blood population and perhaps that helps to explain some of the, the more, res recent findings that we're associating, with some of our diagnostics that we'll come on to later.

And interestingly, just to kind of put a perspective on this, it is important that we understand, what we're dealing with when it comes to the, economy of these horses. And we look at across the spectrum Europe versus USA and the UK. There's in UK one horse for 70 people versus USA where that number is, is, is actually doubled one horse.

For 36 people. And we look at the percentage of, of thoroughbred racehorses associated with that, and it's, it's very low, 1.5% in the UK, 0.8% in the US.

And what I'm really trying to demonstrate with this is that there's a far higher percentage of, non thoroughbred horses in both the US and the UK and also in Europe. Then there are other types of horses, and therefore, what we cannot do is extrapolate the thoroughbred, numbers into our general horse population. Interestingly, from a, a, an economy perspective, the, the, the, the horse population as a whole, and all the associated industries generate between 8 billion pounds and 9 billion pounds for the UK and Irish economy.

It's a massive industry, and I, and I, the reason for this. This is, it will become clear as I, as I go on, and that means that between, the average spent per horse in the UK is something like 3500 pounds is spent on a horse that has already been bought, just in maintaining and keeping that horse in the UK. So there's a lot of money that is spent on horses, and this particular disease, the prevalence of it, 13 in 1000 horses in the thoroughbred population, really begs the question, what are we doing to look for it in other horses?

And this is when it comes to the UK. This study done in 2014 was just an owner survey done by Pet Plan, one of our main insurance companies, and what it's very interesting, and what they see is that the average horse owner is a 4 to 49 year old female who's in full-time employment and spends just under 40%. Of their income on their horse.

And I think that's, that is telling. And, and the reason that's interesting, also looking at the amount of time it's spent 2 to 4 hours per day with their horse, and they ride 4 to 6 days a week, and 84% of the owners in the UK have their horses insured for veterinary fee cover. What we see by that is that these horses are pleasure horses, they're pets, they have money that they can spend, and therefore, what is not really acceptable for a lot of these owners is to be told that their horse has a condition that is not curable or that it does, there's no option for.

And that's certainly, the reason and the basis for coming and looking from my perspective at the evidence base for treatment is because far too many of these horses, vets don't really understand what can be done, the outcome. And what can be offered to hor horse owners. And unfortunately, the, the frequent reason that people are coming to see myself, with horses that are ataxic is because they've gone online, having been told by.

Their own vets that there is no treatment for these horses, and therefore they should be euthanized. And then the owner, the typical horse owner, who is this female horse 49, who has money that they want to spend, or horse is not a commodity, it's a pet, usually something they derive pleasure from. They start looking on Google and they find Actually, no, there is something that can be done.

And why does the vet not know about that? And I think this is a, this is still an issue in, the veterinary industry, the equine veterinary industry today, and, and unfortunately, it's all too frequent. And so, hopefully what I'm trying to do is dispel some of those, Myths that actually we can do a lot with horses that suffer from cervical vertebral stenotic myelopathy, and where owners are committed, certainly the majority of these owners are very committed and want to be able to at least try and do something.

So it it really serves to demonstrate that we're dealing with not thoroughbred horses. They, these horses have a later competitive starting life. Oftentimes they're not necessarily particularly, advanced competitive animals.

The horses are living longer, they're being cared for longer, people are wanting to have a horse that is part of their family. Or part of their, their, their hobby life, and their recreational life, and therefore, again, want to be able to do something if their horse is diagnosed with the condition. We have greater recognition of clinical symptoms, as well as an ability to diagnose, a variety of clinical symptoms that may result in horses becoming intoxic.

And then what, finally just wants to highlight the fact that the reason that also we, we have to be able to really identify accurately these horses that may be suffering from, even low grade, ataxia and spinal cord compression is that if we look at the importation of horses each year, you will see. That in the UK, America, Europe, Mexico, and Russia, there's a large population of horses that are imported each year. And when we look at the export market, when we put the USA in there, the USA have the highest numbers of horses exported to Mexico.

But Holland and the UK have the next largest exportation of horses, and increasingly what are being asked for are net radiographs, and we have to be able to identify as equine veterinarians, those horses that have underlying ataxia and potentially are prone to being low grade wobblers, especially when we see that the warm blood incidence is certainly higher than potentially we have initially thought. And interestingly from the UK perspective, the average UK export value of a horse is $58,000 versus the US average, which is $1900 so we have the highest exportation value per year of horses going outside of this country, into other countries. That.

The higher the, the higher the horse is worth, the more then that is expected of pre-purchase examinations, and the greater that we have to be able to recognise those symptoms that are going to result in, horses that may be prone to, ataxia. So recognition is key, and that that really is key. And when we look at a horse like this, I don't think it takes long to understand that there's no way this horse would pass a purchase examination.

It's very weak behind. Look at how it steps, it cannot step in the same position without being, stumbling or putting its limbs in a, in an awkward position. As it's turned, it, it struggles to turn its neck round, it would rather back up.

It drags its toes and it, and it steps on itself, and it nearly collapses behind each time it's weak. And I don't think it's hard to say in this instance that this horse has is a toxic and is a cause for concern. I think that's fairly readily obvious.

You can look at a horse like this, and this horse has an unusual gait behind you would maybe question its left hind limb saying, yeah, we've got a bit of left hind limb lameness here. As it comes to the end of this trotter, just have a look at it go in its hind limbs. You can see it that it kind of bounces along as it goes, and it has this almost slight spring in its step as it goes, and it looks like it's just a, it kind of looks like it's been sedated on, on a slightly, slightly sedated look.

Now it has a mild circumduction of both hind limbs, but again, as it comes back towards you, just look how the, the step, it's. Slightly bouncy, and it has that slight, hypermetric stride. And, and that's an important thing to recognise in a horse here, in which hypermetria is, is a little bit evident.

And you look again at something like this. This is a 4 year old stallion, it's a fairly old video, but it's a 4 year old stallion, and every so often it, it circumducts or abducts it's either one of its hind limbs and. Other than that, aside from that, it, it is completely apparently normal.

It's a, as I say, a 4 year old stallion, and it, it walks, as you can see, it flicks its left hand and then it'll flick its right hind. Just slightly add ups it and this horse here. Has a C6-7 compressive lesion, and the only evidence of that, at least in this dynamic exam phase of the horse, is at the walk when it has that funny gait.

So really we have to be able to start looking at the more subtle findings as being evidence for a horse with potential spinal cord compression. And so that really brings me to then the neurological examination, and you can see this horse here, which can, as it's been turned the neckli is not bad. However, it struggles with to, to, to turn round on itself without either circumducting the hind limbs or stepping on its fore limbs.

And we do a bunch of different tests really and all all these tests are, are doing is, is to evaluate, does the horse know where its legs are in relation to its body. Here you can see again circling that big wide step out. And then it kind of steps on itself in front.

In the backing up phase, it can back up OK, but when it comes to halt, it doesn't really know where its legs are and and the legs are not replaced into a more normal position. And you can see that with changes in speed or direction, the horse can't, doesn't really understand and can't cope with that. The tail pull exam is an important part with them, with classically ataxic or spinal cord compression horses being very easy to pull over to one side.

And you can see this both left and right, the horse is looking relatively relatively weak on, on the tail pole as it's walking away. And this horse is this horse here has a C45 compressive lesion of its spinal cords. So really the neurological exam is designed to, it's designed to test the horse's ability er to respond to normal er reflex actions when tested going up and downhill, changes in speed and direction, or doing things that are going to test whether the horse's normal reflexes and ability to pick its legs up are challenged.

And when it comes to the European presentation, the, the, the two studies that have been done really is an overrepresentation of males versus females, and again, pleasure horse and sport horse predominate, the European and, and the UK population of horses. Our own study backed that up with the mean age. It's been 5 years.

Again, a higher proportion of male than females, interestingly, and what you can see again is that the presenting signs typically are not necessarily all ataxia. These are all horses presenting for, some degree of neurological, abnormality or gait abnormality. Ataxia as a feature is only present in, in, in just over a third of these cases.

So, in other cases, it's lameness, that's the main presenting site. Hypermetra often present. Stiff neck, less common, tripping, weakness, some of these symptoms, but by far and away the most common presentation for horses that are presenting for neurological symptoms is either ataxia or some degree of lameness or gait abnormality.

And when it comes to gait abnormalities specifically, then they, it can be generalised and 4 and hindlimbs or an even distribution between 4 and hind limb gait abnormalities with just under 0.5% with no gait abnormality at all. And of course some horses are neurological and lame.

You can see in this instance here, this horse has a bouncy hypermetric gait behind a six year old show jumper. The horse has been show jumping at at at a relatively high level, but the problem has become lame, so it cannot pass a trotter. You can see here that it's got a right front limb lameness as it comes back.

It looks like it's a bit bouncy, and this horse has a C4-5 compressive lesion, as well as a radiculopathy at C67, and we'll look at that in just a minute. So some horses are neurological and lame. And then I just want to show you the presentation that we can see, in, in some instances, which has been described as being an idiopathic hopping like lameness by Sue Dyson.

You can see this, this is a seven year old, dressage, warm blood horse, and on the right rein, you know, moves pretty well and is, is coping nicely. But when we go on the left rein, what you'll see is an intermittent, right forelimb lameness on the left rein that is there consistently. And this lameness is Always seen under saddle on the, with the affected leg on the outside, and the horse has been blocked up to including the level of the shoulder joint with no apparent change in that degree of lameness.

And this is typical of what we call an idiopathic hopping like lameness, a rhythm lameness, seen with the leg on the outside of the circle. This presentation. As I say, has been described, and we increasingly recognise as a result of CT analysis of these nets that these horses are suffering from some degree of nerve root compression or what we call radiculopathy.

And Sue Dyson wrote these up, back in 2016, and, you know, looked at a total, her, her, her presentation was a shortened cranial phase of the stride, with marked elevations of the head, and as the forelimbs protracted, we typically see it on the outside of the circle. And, you know, there's no history of trauma in these instances, but there's a reduced performance and an intermittent to moderate lameness, again, only seen under Saddle, and really no conclusive diagnostic tests being done from her perspective. Now she didn't have CT available to her, so none of these horses have been CTd.

However, she did, follow them up and out of the 25 horses, you see that 74% of these horses are exacerbated lameness, with blocking. And, very often, radiographic abnormalities in, in just over 90% of horses are seen on C6 to T1. Now it'd be lovely to have CT analysis of these, which we can now do, obviously, and is relatively common, across centres in the UK.

So, . However, on PM of 3, on PM of 25 of these horses, only 3 demonstrated true nerve root compression, histologically, and so it begged the question of really what's causing these, however, I hopefully we'll demonstrate soon just what we think is going on. And this is typical of a horse, you know, this is a very severe, lameness here.

You can see just how markedly uncomfortable this horse is, here on the forelimb and really doesn't look like using it. This horse has major, degenerative joint disease of the C6, C7 articular process joints, and specifically on the left side, where it's massively, enlarged articular process joints, resulting in nerve root compression. And so when we see these hopping like lamises, you know, we look at the anatomy that we're looking at, associated with the vertebral foramen, and you'll see that when we, you've seen this image on the left before, when you have remodelling of bone, the remodelling of bone can happen anywhere in that joint surface, including the ventral aspect, what we call ventral buttressing, or all around the dorsal aspect.

But if it affects the ventral aspect, the nerve root comes out at the ventral foramen. And that intravertebral foramen at that point, where the nerve root comes out is very susceptible to being compressed by bone and therefore resulting in some degree of nerve root inflammation. And if nerve inflammation occurs, then it is the equivalent to the horse of having, a trapped nerve.

And I think that's, that's the kind of, pain that you often see with these horses, when they're as severe as the one that you've just seen, in the previous slides. Here you can see that the remodelling can really start to impinge down, on the nerve roots, the nerve root exits the more caudal aspect of the invertebral foramen. It's not hard to see how with bony remodelling, this can become a, a real issue.

And on a CT exam where you can see normal invertebral foramen, you, you start to see with osteoarthritis, little osteophytes that appear both on the axial as well as the, the avaxial, aspects of the articular processes and that blue. There where it's saying narrowing of the intervertebral framen. Well, you can see the space on the associated with the, the, the right hand side of the intravertebral framen compared to the left hand side and sometimes it can be quite dramatic where these nerves become very compressed due to the bony remodelling.

Here's a diagram taken or demonstrating where the spinal cord goes through the intervertebral, the spinal cord goes through the spinal foramen with the nerve roots exiting the intervertebral framen. And again you can see where the joints, where there's bony impingement or enlargement or remodelling on the ventral aspect of the joint surface, it will start to impinge, put pressure on the spinal nerve roots. And you can see in this instance here how just severely collapsed these, and severely narrowed the invertebral framen becomes, and thus how quite clearly you can see the spinal nerve in this instance would be severely compressed, resulting in some of the symptoms that we then see.

So when it comes to the presentation of clinical symptoms, how, and how we recognise these horses with spinal ataxia, very important that we recognise it can be all different types of breeds. Typically, thoroughbreds have been overrepresented, but only because they've been the ones that have been reported. Warmbloods, in our proportion in the UK certainly seem to be overrepresented with the older horse population presenting as a static.

Degenerative joint disease as opposed to a dynamic, malarticulation, type of problem. We see that the pleasure stroke sport horses predominate the case load with gelding's overrepresented, and there's, there's a severe under recognition of the more mild forms of, of ataxia, with both owners and. Vets out there.

And when we see that greater than 50% of these subsequently confirmed, attaxic courses were referred for non neurological symptoms, we just see that there is an issue here with, with recognition and, and, and, and that's not something that I say lightly, it is something which we all, can really learn, and train ourselves to recognise. And that leads me on to the diagnosis. You know, typically, from my perspective, this is, this is the typical, pattern that a horse is presenting with either poor performance or a gait abnormality.

The lamest examinations and neurological examination happen concurrently with each other. If the horse is lame, it's very important that the lameness is, is worked up properly and effectively with, the, the usual lameness diagnostics and possibly nuclear. In geography.

If the neurological examination is, is positive, and to some extent, then really we go down the plane cervical film routes, and then if they're positive, we go down to myelography and, and nowadays, contrast enhanced CT myelography is really the gold standard. We can ultrasound these, and have a look at the joint surfaces, horses that have stiff necks where funds maybe are limited. That, you know, ultrasound can be useful.

However, there's no doubt that from a, from a sort of gold standard perspective, and I think now, if we look at the predominant horse population, 84% of it being insured, then, you know, it offers a very comprehensive, way of evaluating the, the, the cervical spine. And, really, in, in, and certainly in our opinion, what. MRI has done for recognising, conditions and issues within the foot.

We consider that CT and contrast enhanced CT now helps us in the same way to recognise, conditions and pathologies associated with the cervical spine, and certainly it has dramatically, increased our understanding of the reason for this disease and, and these horses demonstrating ataxia. But interestingly, you know, when it comes to recognising these horses, what we, what we know from, from, Richard Pearce's group study done in 2014 is that a grade 3 wobbler is really where we get unified opinion. The the more subtle signs associated with grade 2 and certainly grade 1, Ataxic courses, we see a tremendous spectrum of those being either missed or being accounted for something else we want.

And there is some degree of bias here, but there's a significant variation in in grading. But what we do know is that once they get to a grade 3, which is a horse that's consistently demonstrating weakness or ataxia in the hindlands, then we are probably on the same page as being able to identify these horses. And radiographically, you know, there is a problem because there is plenty of scope that, enlargement of articular process joints does not necessarily indicate neurological deficits or neurological disease.

And, and we know that, because there's a huge variation in the size of the articular process joints, particularly as we go down to the base of the neck, . And the other sort of very important factor to mention is the fact that radiographs oftentimes can be underrepresenting what's going on, but also we can overinterpret radiographs due to what looks like, artefacts, well, sorry, what looks like pathology, but it's actually due to positioning when we get overlapping of articular process joints that sort of make our articular process joints look larger. And what we know from Fran, Henson's, paper is that, you know, as horses get older, there's a, there is an increasing enlargement, associated with more caudal antic process joints, and that can obviously lead to difficulties because then these horses, are presenting the tax to off.

Sometimes it's the C67 that we're looking at, and, and yet in more normal horses where there's no ataxia, we can see enlargement of these joints. It's not necessarily meaning that we're not, that they're not clinically rele that they're not relevant, it's just that they're not clinically manifesting themselves at this point. An important take home point, you can't diagnose a warbler necessarily from playing radiographs, you can get some idea by doing, Caroline Hand's NICE study when she looked at the intervertebral and intravertebral ratios.

And when we measure A over B, which is the narrowest part of the spinal column over the widest part of the vertebral. If, a, a value of less than 48%, that ratio less being less than 48%, has about a 90% positive predictive value of, of having narrowing of, and therefore compression of the spinal cord at that site. And you've got this greater than 52% as normal, which often then leads to this grey area between 48 and 52%, which we're kind of left a little bit unsure of.

If we're doing this alone, then, you know, this gives us some indication that potentially we're dealing with a horse. It has spinal cord compression. However, clearly there's a big cohort of horses in which either the, the, the measurements are not measuring just quite at the 48%, but they're also not greater than 52%, and it's those horses that really we need to be, more confident about diagnosing.

That's where myelographic myelography comes in, and traditional radiographic myelography gives us a greater indication certainly of spinal cord compression. The typical measurements used are the, are the decrease in the dorsal contrast column, and, you know, by 50% and, up to 7 and then 60% C71. If there's a reduction in the dorsal contrast column, and you're really, you're measuring that in the middle of the vertebral body, the, so the dorsal contrast column in the middle versus it over the, where the articulation is between the two vertebrae.

In conjunction now increasingly as well with the reduction in the total dural diameter. So if we see the dural diameter in the middle of the vertebrae decreasing by 20% compared to it being, compared to the measurements at the junction between the two vertebral bodies, then again, that gives us a greater degree of confidence that we've got a horse with spinal cord compression. Importantly, the myographic views and we still are very, we're still very keen for these myelographic views radiographically, even with CT, looking at the flexed and extended views, very, very important.

With dynamic compression, we will often see a normal dural diameter and contrast column in a neutral position, but when we flex, in the case of The C3, 4 and 5, and when we extend in the case of the C6, C71, then that is when sometimes we more commonly associate with horses with compressive lesions at these sites, that's when we're gonna see it. In the middle of the neck, in a horse inflexion, an extreme flexion, that is, and the caudal neck with the horse's neck in full extension. And so you can see here the dorsal contrast column being greater than 50% reduction compared to it being in the, in the middle of the virtual canal versus the total dural diameter decreasing in size by 20%, as you can see.

So the problem with radiographic myelography, as I'm sure you can very much appreciate is the fact it only allows us to identify dorsoventral compression does not allow us to evaluate lateralized compression. It is a 2D imaging process and the specificity is and sensitivity is, is low, between 43 and 76%. That means we miss horses that potentially are actually truly, have compressive lesions, but also we may well over, estimate those horses that are actually normal.

So there's only a 68% correlation with knee cropsy, so we underestimate more often than not, spinal cord compression. Plus, we don't really see a lot of pathology, and this is where CT has really come into its own in helping us to understand the components of pathology that we previously do not recognise due to the two dimension. The nature of a radiograph and the dorsoventral and lateralized compression is very clearly evidence, using CT for obvious reasons, we're getting three dimensional multiplanar cross-sectional imaging with a far superior imaging quality, and we can see underlying pathology far greater because the radiographic anatomy is separated out.

And I, this is not new. I mean, I think the ability to do it in the live horse certainly is, is much more recent, but Bonnie Rush back in 1992, demonstrated that CT can be used to, to, to, to evaluate these stenotic horses. And, and we certainly in the early days, you know, when, when, when we had a CT, this is way back this, this is about 9 or 10 years ago in, in our old system.

And this, this gantry is a 45 centimetre, boar, so, and really, we experimented in different ways of trying to get the horse's neck in, but we couldn't do it. It, it, we got down to C3 or C4, and that really is hopeless because the majority of our horses with, compressive myelopathy or pathology in our older horses, and it's nearly always the, the caudal cervical vertebrae that are affected. And so, Mats Christophersen brought this very nice, study at Viava Congress, in 2014 demonstrating just how to do CT myelography and using a 90 centimetre bore, and that was very nice, and that led us, in 2016 to get our own, CT and then reports on our cases last year, over the course of two years, looking at 51 clinical cases.

And, and this is really what, how, how it's. Done. So, you, you know, the horse is is placed now in lateral recumbency, that 8 cm bore it is pushed right into the CT unit.

You can see the horse's head coming through the other side, and the laser lights down at the level of the shoulder region and this allows us to get down consistently down to C71, on any size of horse. So, really, the warm-blood horses, some of the bigger warm-blood horses, we should, there's no reason for us not to get down to T1. And you can see here, this is, you know, when we first started doing it, just, the horse's shoulder is right off the edge of the, of the table here and it, you know, the, the horse's head and neck, they're on triple drip, they are really.

Yeah, it's a relatively straightforward procedure now thanks to the fact that we, can, can get through it fairly rapidly. This is the positioning of the horse again. You can see the laser lights down at the shoulder level scapula here.

The horse is on triple drip, has oxygen innasally. We do put a catheter in. Monitoring blood pressure quite a study to see what happens, fluctuation of blood pressure once, injecting a contrast, and so that's the position of the horse, and it's fairly, it's a lateralized procedure.

It takes roughly about 20 minutes to complete and start to finish. And the, from the actual procedure itself, it, it, I'll take you through how it's done, so the horse's head and neck is elevated, we do an a tap, and we take, CSF out of the, spinal canal, so we're getting approximately 50 mLs of spinal, er spinal. Fluid out.

And by doing that, really then replacing that by injecting, we inject 20 mLs of, of neat contrast in, and then another, 30 mL, of contrast mixed with 30 mL of sterile saline, elevate the head for 5 minutes and then scan through the CT scanner. And here's, I put the sound on just to help you understand this is looking through. This is the horse going through the biological procedure.

It takes about 40 seconds for from start to finish for the CT to, to run, so the horses left, for 40 seconds to have that procedure performed. The whole procedure takes about 20 weeks. And this is what we're going from.

We're going from, a series of, of radiographs, and a radiographic myelogram that, you know, allows us to see nicely dorsoventral compression, but obviously also looking then when it comes to CT you have a much clearer image, both sagitly as well as on a transverse plane here. The CT very nicely demonstrating contrast on a circumferential basis around the spinal cord and. And quite clearly you can see the advantages of, of this technique.

So what we found in our particular cases, you know, a lot of different things, particularly in vertebral frame and narrowing osteophytes and enlarged articular processes, multiple things really reported and, just take you through some of these, you can see the osteophytes on the lateral aspects, so they have actually. Aspects of the articular processes. They're quite pronounced, but, and the articular margins here, you see the myelogram image on the right-hand side where compression is not a feature.

And degenerative joint disease, we, we graded, with, from a 0 to 3 with, and, and really the, what we saw is that, you know, Well over, well, nearly, nearly all horses had some degree of evidence of, of osteophytes, with 44 or 51 having grade 2 or greater. And the key question always comes down to, OK, what is it that we are calling significant when it comes to Clinical disease, we call grade 2 and grade 3 significant. Those horses have irregularity of bone, they have enlargement of their articular process joints and have clinical indications of neck stiffness, neck, articular joint enlargement, or pain on the neck.

Osteochondral fragments are now very well recognised as a result of CT. We can see on radiographs something like this, and in 11 of 51 horses we recognise these, and they can be quite large, up to 2.5 centimetres in size, and you can see them very clearly here.

And this is important really because, as Russell Parker and the group at Lite Pook have demonstrated quite nicely, and Rachel Tucker and Roger Smith, before that, arthroscopy for such fragments can actually be done. You can see on this image here, the CT study demonstrating quite nicely the ostochondral fragments, on the dorsal aspect of the joint, and this can be removed arthroscopically. The ones more ventrally located, unfortunately cannot be removed, but certainly these dorsally located ones can be removed like any other OCD fragments.

And as I say, arthroscopic evaluation is, is, has been well reported now with Rachel Tucker, being the being and, and Roger Smith demonstrating quite nicely the, arthroscopic approach, and. The study done before that really looking at the anatomy of the cervicortic process joints, just highlights why these joints can be particularly problematic for the horse. They, they, they are large joints and they have these multiple thick synovial folds in them that bleed.

And when they bleed, they bleed like any other joints and cause a hemoarthrosis, and then that settles down, they become fibrotic, they get a synovitis that then results in a synovial hypertrophy that becomes a stiff, thick synovial lining, and this then results in restriction in neck movements and pain. So. When it comes to arthroscopic treatments, you know, in a younger horse, Rachel Tucker, as I say, reported this one from, the Royal Veterinary College when she was a resident there.

And this, this little colt had reduced lateral neck flexion, no gait abnormality, no paresis, no ataxia had just reduced lateral neck flexion and walked with a stiff and extended neck. And I think the important thing is really that what CT highlighted was a nice big fragment and ultimately speaking, these fragments, like I say, can be removed. This is a, a, a nice, example of an a fragment you can see arthroscopically on the right hand side of the screen and the group.

From Liook nicely demonstrating how arthroscopically these, these fragments can be readily removed. And, and they're not frequently common, 11 of 51, certainly with the Russell Parker's group, there was, they, they had 5 of 11 horses, that were considered clinically significant, and, 51% of their, sorry, 31% of their horses that were myelogrammed had some evidence of osteochondral fragmentation. So important that we are are are recognising the fact that horses, just like in any other joints, the cervical joint is, is, is affected by conditions that we can do more about now.

And it's not a matter of saying, OK, we've got a, a big fragment there, that horse has got a stiff neck, therefore, or it's got reduced neck flexion, or it's tripling with something, and we know that the joint's affected, not a matter of saying, well, actually that's it, can't do anything, no, these things can be done and should be done. When it comes to dorsoventral compression, the myelography part of the CT, you know, here you can see satly how nicely CT will demonstrate that, and certainly the myelographic findings from our study, demonstrated in, in just under half of the horses, no compression at all, with a sort of roughly distributed, compression affecting C67 and C56 across the board. Lateralized compression interestingly was seen in.

Approximately 80% of these horses, to some degree. And remember that, that, just over half of these horses were presenting with, symptoms of, gait abnormality, lameness, as opposed to ataxia. And so in that respect, then, when we see lateralized compression, we start to understand just what it can do to horses when they are, have some degree of arthritis that's then impinging on the lateral aspects of the spinal cord.

And here's an example of lateralized compression. This is relatively mild versus the middle picture where it's markedly severe, and this, and, and has a, a profound, effect on actually reducing, not just reducing or or ob obliterating the, the, the contrast column on that lateral aspect, actually impinging right into the spinal cord. When it comes to management, you know, and the, the distribution of, of the static lesions, again, what's interesting here is that the, in the warm blood horses, the, the static lesions certainly usually associated down at C67, but also there were dynamic lesions seen in about 20% of horses at C45.

Our our case population certainly with pleasure horses and, and, and a lot of warm blood horses, we, we probably our cases are far more related to the C67 C71, with C45 being less commonly indicated as as a site of interest. But interestingly, don't, in, in, in the, the main point being here, that horses don't necessarily demonstrate neurological signs until they're older, despite having dynamically compressed compressive lesions. And, and, and that's perhaps a reflection of the fact that these horses are not being trained and not entering any sort of work until they're more mature.

And so we're just not recognising these clinical symptoms until they're actually starting to be. The horses are starting to be put under a bit of pressure, and then just like any other OCD or any other arthritic type lesion, the more these horses are working and exercising, the more prevalent these things are seen. And when it comes to the number of myelographic sites of compression, interestingly, 15 had no evidence of myelographic compression, and the, and the, and 35% had had 2.

So roughly distributed, you have 0 in a third, you have 1 site in the third, you have two sites in a third. And interestingly from a radiographic myelography, they this group reported 85% being diagnostic. Our our numbers certainly would be less than that based on the radiographic myelography.

With the CT myelography, where we're identifying lateralized compression, we think we have a far higher ability to recognise these horses, especially where the compression is, is less than 50%. So from a conclusion, the contrast enhanced CT really allows us more accurately to identify the exact cause of why this force might be toxic and therefore direct our treatments to be more specific to the specific lesion that's identified. And if that's arthroscopy or If that's fusion, or if that's neck medication, we're far, we're, we're therefore far more likely to be able to orientate our treatment towards the horse's problem as opposed to a blanket treatment for, for something that we're not really sure is necessarily going on due to our issues with, incomplete diagnosis.

From a treatment perspective, what we're really looking at is now the evidence base for treatment, and that really, again, the, the key thing for treatment and identifying, or rather, being, accurate or most successful with our treatment is obviously that we are accurate and able to identify accurately our pathology. And so our treatment aims are really to reduce the acute and ongoing inflammation of the spinal cord, to prevent compressive episodes affecting the spinal cord, and prevent further degeneration of the articular process disease or arthritis, which are fairly broad aims and also with the specifics of this nerve root compression to actually identify and not only identify the fact nerve root compression is happening, but then. To try and do something to prevent it.

And really our three broad treatments, within cervical spinal pathology are arthrodesis of the spinal cord, spinal, vertebrae, medication of articular process joints, or arthroscopy to remove articular, osteochondral fragments. And the question that always is posed is should we treat these horses with stenotic myelopathy? This horse here is a horse that 9 months prior to this was a grade 5 out of 5 ataic founder in the field down and could not get up.

And it subsequently, after steroids was able to be transported to the hospital, where it was slung over the course of 3 days, underwent a myelogram and had severe compression of its spinal cord at C6, C7, C7, C1. Now with this use of a sling, it was supported, it went through surgery, it had its C67 C71 fused and was in a sling for two weeks post surgery and then was gradually. The sling was removed and 9 months post surgically surgery is now like this.

Admittedly, it's not a normal horse neurologically, but it certainly is not a grade 4 or even a grade 5, ataxic. Really, I use this as an example of a horse that an example of what can be done with horses, and I'm not suggesting that every horse has this done, this, this owner is very committed, this horse is a dear horse to her. And she falls into the bracket of people that I mentioned before, who, for them, their horse is part of the family, and they're not content with the option of just euthanasia if a treatment could be performed.

Now obviously horses that are grade 4 and grade 5 present unique challenges with respect to surgery. Owners have to be very, very aware of what surgery involves and the longevity of the time it takes for horses to recover. And obviously it depends on the number in the sites affected, the length of rehabilitation time, but also what I want to try and .

Very much try and underline is the fact that. We have no problem treating horses with fractured legs and accepting the fact they're going to be 69, 12 months out of action, and maybe lame after that. And in this respect here, really, I don't, I put these in a similar category.

These horses may well take 36, maybe 9 months before they can be ridden, put a saddle on. And in some instances may not be able to be ridden, but in most instances can undergo a ridden career, and the commitment of the owner and the expectation of the owner has to be tapered towards a time lag, a time length, in which they're realistically going to be rehabilitating the horse, but there should be no doubt that something can be done for them. Which is that's why I want everyone here to remember this slide that we're dealing so commonly with horses nowadays that for which the owners, it's their source of pleasure and their joy with with 96% of horses in this country.

Being pleasure, stroke, low grade competition horses. And I put this in because I want to highlight the fact that, you know, conservative treatments and surgical treatment as an option should, in my opinion, be far outweigh the number of horses undergoing euthanasia in these instances. In the European study that was done, 47% of all cases were euthanized.

69% were conservatively treated and improved clinically and ridden, and these horses were mildly attaxic. They were grade 1 and grade 2. They had evidence of articular joint pathology, but minimal evidence of, .

Compression of the spinal cord. And the conservatively treated horses, about 70% of these improved clinically to the point of being able to be ridden. The surgically treated horses were treated, there's a relatively high proportion of horses with, thoroughbred horses, under 2 years are euthanized, and, and that, that really represents the The industry, that obviously these horses are seen as being not useful if they're ataxic in any way, and I understand that completely.

However, we have a relatively high success rate in these young thoroughbred horses, which have dynamic lesions and for which actually the compression is only seen in a flexed neck position. And so when that neck is fused in a neutral position, actually there's no spinal cord compression at all. I'll take you through some of the numbers.

In this study, 8 of 14 surgical cases were euthanized, and I think that's a very high number. Our own experience out of, 22 horses, 3 have been euthanized, due to, various things which I'll, again, we'll go through in a minute. In our cases, 51, 90% of horses were treated post CT and intra-articular medication and 46%, 7 of 16 stenotic horses had cervical arthrodesis, and 6 out of the 46 horses were euthanized.

Subsequent to that, we've, we've done another. 6, cervical, fusions, and none of those horses have been euthanized except one, which is a triple level, that didn't recover from anaesthesia. It was a grade 4 prior to its, surgery, and that really didn't, it, it didn't get up.

Now, I, I use this slide really to demonstrate that that post CT myelography, really what we're seeing is a is a roughly half, sorry, 2/3 of horses with some degree of arthritic changes that we're treating conservatively with medication. And a third of horses that have stenotic myelopathy that then half of which owners choose and elect to go forward with cervical fusion. But what's the evidence for interbody cervical vertebral fusion?

And this is really talking about the basket surgery, so water surgery where we are fusing, removing the disc between the adjacent vertebral bodies and placing a titanium steel basket with a bone marrow graft placed in that and allowing that vertebrae to fuse. Now, if we look at all the papers that have been produced, and there's not that many, in 1993, greater than 1000 horses had had this procedure performed across the world, at least reported. But really in 2020, there's, there's well over, and this is a low grade estimate, 3500 horses.

Doctor Barry Grant, who's the pioneer of this surgery in the United States, he himself has done in excess of 2500 horses. So, you know, this, this is a tried and tested technique. It's been done over 40 years now.

John Walmsley, who was really the, the grandfather of the technique in this country, demonstrated that he, he commented that the thousands figure in 2007 being well over double than that, and certainly, by, by conservative estimates there's been well over 3500 that have been done. If we look at the reported cases between 1983 and 2009, they cover a range of disciplines aged 3 months to 26 years old, grades 1 out of 5 to 4 out of 5, both dynamic and static, presentations of CVSM, and with a recovery time of 6 to 18 months, but I really want to demonstrate is the two, the two UK studies here, the, the. Richard Reardon's study where he had resolution of ataxia, in a 3 month old fall using a walking compression plate.

But more importantly, John Walms's study in 2005, in which about 61% of horses returned to their intended use. And that, that would fit, you know, these, most of the Walmsley studies, worms the horses were warmbloods. Very few were, thoroughbreds, and so these Warmbloods were the horses that we're talking about with more arthritic type of degenerative changes within the joints, and a 61% of these horses returning to intended use.

You look at the racehorse population, which the majority of the other studies are talking about, and there's between, sort of 60 and 80% of, success rates in horses returning to training in these instances. When it comes to discipline, the racing, certainly 46% returned to racing or race training in 1993, but in 65%, Barry Grant reported in 1985, and really that's the, the, the most recent study that's been done of any significant number of horses, and that's needing updated, you know, that's clearly that, that study is over 30 years old now. John Walms in 2005 reported that a 5 of 8, Thoroughbreds trained and raced, which is a 56%, sort of overall, return to racing for these horses.

By Grant reported triple level, 75% of triple level horses trained and raced with 2 or 4 winning. In terms of ridden or breeding animals, the, the success rate's obviously going to be much higher, with, between sort of 56% and 83%, and an average or mean success rate of 71% of these horses returning to some sort of ridden or breeding work, and depending on the number and the site of pathology. In terms of the site of lesion, if C34 was involved, that's typically these young horses, dynamic compression success rate is slightly higher.

So 63% John Walsy, 77% return to work, of the C34 lesions. The C6-7 lesions typically are the horses with more static changes, arthritic type changes, and in those instances you're talking. Between sort of 50 to 60, 60%, will have, a return to, some degree of written exercise.

And the typical statistic that we quote, most owners now is that, is, is that roughly 50% of horses will improve by 2 grades of a taxa with just about 80. Percent of horses improving by at least one grade. So I think that's an important statistic.

It's the one that that we tend to use from any toxic perspective. Horses with confirmed stenosis of their spinal canal will improve with cervical fusion by about 50% in by 2 grades and 80% by by 1 grade of ataxia. And in this, this, this, this statement about the slow recovery but regression of arthritic changes on on radiographs, it's been demonstrated nicely not just radiographically but also by CT where we see that there is truly, when a, when a joint is diffused, there's regression of.

Arthritic, degenerative bone that then, the bone atrophies. And, and that's true in any fusion process, whether it's a pastor and a hawk, the bone, the bony remodelling actually, regresses to the point that then we end up with a, spinal column that is sufficient room for the spinal cord. So overall, C67 we're looking at about a 65% improvement in horses in that with spinal canal affected.

In terms of the multiple levels that are involved, the double level, it's not a specified, different outcome, and really there's there there's no real numbers in that, but pretty much the opinion is whether you have a, a single level or a double level, it doesn't make that much difference in terms of the long-term outcome. In terms of triple level cases that was reported by Barry Grant, in 2007 and Nick Chuggin. They looked at the triple levels.

11 of 12 horses had a single horse, and 2 of the 12 were euthanized. 6 of 12 had a stiff neck postoperatively. All of the survivors improved by at least 1 grade, with, 8 of 10 survive virus improving from a grade 3 to a grade 1.

And these horses, 2 or 4 racehorses, trained, raced on one, and it really on one horse where they did a repeat myelogram 4 years post-op, they had triple level surgery with no compression demonstrated, which again just demonstrates the fact that the, when we, when we fuse these vertebrae, the, the spinal canal cannot then recompress the spinal cord. So. That's, it, it, it, I think the statement that that is made at the end of this paper is, is, is key.

Affect patients can live productive and or competitive lives with no danger to themselves or their handlers without requiring daily medications. Now when you can make that statement, then that's a pretty powerful statement, and we think of the number of horses that are on, buttes or on analgesics in some way, shape or form to keep them. Sound, and we see that in these instances, these horses that actually live a pain-free, life without the need for daily medication and can safely be ridden in between 60 and 70% of cases.

Really, we have a pretty compelling argument for saying that cervical arthrodesis is, is a valid and should be a, a, a technique that's presented as an option to owners. So in summary, from a cervical arthrodesis perspective, it's a validated evidence-based supportive technique and it does alleviate spinal cord compression. The body of literature supports its use, and from over the past 40 years now, we don't have.

We don't have sufficient data, but we've got enough data to demonstrate, especially more recently now, that over 250 reported cases over 40 years support the use of cervical arthrodesis, with conservative treatment being used for very young horses, and, and I say conservative in, in the instance of Cervical vertebral myelopathy, where we're getting stenosis, where there is true stenosis of the spinal spinal cord, then very young, very mildly toxic horses may well respond to, dietary reductions. But the majority of horses that have stenotic myelopathy, if identified, can be operated on, successfully. And importantly, there is no current reports of horses that subsequent to their cervical fusion have had accidents, at least that, or that we are aware of, where it can be demonstrated that that because of their procedure, they have then ended up being unsafe.

Now, in terms of conservative treatment, where there is no evidence of spinal cord compression, but there is evidence of articular process, enlargement or arthritis, then articular process medication really is a, a very valid and and well now established tech technique. You know, ultrasound guided articular process injections, is, is very commonly done by many sport horse practitioners, including ourselves, and, and again, in instances where there's either mild lapsized compression or where there's no compression spin. Or, but we've got evidence of enlarged, or arthritic spinal, articular process joints, then this is a very valid technique.

It's been reported in two cases. The evidence base is, is pretty strong for its use out of America, . The, Steve Reed's group demonstrated that, out of, the, the horses that had, single treatments of methylprednisolone, acetate, plus or minus HA and some amiccain, they had 32% were resolved, 39% had an improved performance, and 50% improved for between 1 and 6 months.

Interestingly here, 60% of 33 Ataxic courses improved two grades of ataxia for between 1 and 5. Now, these horses were being identified by Steve Reed, who would, possibly have the the sharpest eye in the world for antaxic horse. So potentially identifying horses that are grades 1 and 2, and then, horses there that are, being medicated.

I, in this instance, there's the, the, the, the inclusion criteria for those horses in the Birmingham study, less strict. And then, Dickie Hepburn's, nice retrospective study looking at, horses that had, all of which were neurological, all of which had neurological exams by him, and all the success rate being defined that all limbs, were a neurological grade of less than 1 after treatment. And in this instance, the horses that were greater than 8 years old.

Had neurological signs and radiographic changes. There was no myelogram, but 80% of them improved or resolved by two grades. It took 1 to 4 months for signs to resolve, and, but the, the, the resolution was, was significant for between 1 and 5 years, and repeated treatments, generally speaking, carried a longer term success.

In the instances where the 4 to 8 year olds horses where there was no stenosis on the myelogram, 60% improvement was seen. And again, you know, here, all the horses were neurological, serial rads demonstrated no progression of osteoarthritis. However, the argument really is how easily do we see progression of, of osteoarthritis on radiographs, nonetheless, In these instances in which we are seeing some degree of mild ataxia or mild stiffness of the neck or areas horses which had demonstrate a myelogram, no evidence of spinal cord compression, then we can expect a good response from medication of the, of the articular process joints.

And in conclusion really then, you know, we want to be able to identify horses that have. Cervical pathology, and cervical pathology now really is not just ataxia, and the important message to take home from this is that when we have a horse as a gait abnormality. Of some sort, or we're we're seeing that there is some degree of unusual gate action, maybe one, maybe two hind limbs, maybe the horse has a thinner neck.

That we need to be aware of the fact that a brief neurological exam as part of a lameness examination may just highlight some more subtle symptoms of spinal cord compression or cervical disease that then we need to be able to pick up to then identify and therefore treat. How are we making the diagnosis? The important thing is from a stenosis perspective, spinal cord compression, really CT is now the gold standard for identifying pathology, both whether it's causing a stenotic cord, or whether we have other cervical pathology that that radiographs are not going to identify.

What we need really going forward is to not just be able to identify pathology but to know the significance of that pathology and we're getting there. There's now, there's now 3 centres in the UK that were that are performing CT, studies off the neck and so the and and now, . 6 centres across the world that are doing it, and there is.

Pretty good understanding developing of what is significant pathology and what is less significant. Our definitions of our definitions of success may vary. A return to work versus a return to previous intended use and owner perception.

But what we have to be very aware of is the population of horses that we're treating and that we're diagnosing, and that we have options that we can relate to owners when it comes to cervical disease. That give owners much more hope than previously has been explained or described. We need to continue development of lesion specific treatments, and by that what I mean is there are ways of doing things that we are currently exploring, be that needle arthroscopy of the cervical articular processes, be it the articular arthroscopy rather of the and removal of ostochondral fragments.

Be it to evaluating the reduction of the, remodelling associated with the intervertebral foramen by using, a basket to fuse the cervical, vertebrae. And we can expect in horses with stenotic myelopathy a good outcome for cervical arthrodesis. I hope that's done something to help just gain an understanding of where we're at when it comes to cervical stenotic myelopathy and cervical disease as a whole.

And I'm happy now to take any questions and I will turn on my lights as well. Jonathan, thank you very much for that, very, very insightful presentation. And, certainly, it's amazing to see what what you guys are, are able to do and the fantastic results that you are achieving in these horses.

So, thank you for your time and thank you for sharing that with us. Yeah, no problem. A quick thanks again to our sponsors Bailey's Horse Feeds.

And I'm afraid we have run over tonight, but I hope you have all thoroughly enjoyed this. And if there are any questions, we will ask the office to email them through to you, Jonathan, because as I say, we have unfortunately run out of time. No problem.

But thank you, everybody, and thank you all for attending. And from myself, Bruce Stevenson, it's good night.